The Experts below are selected from a list of 5505 Experts worldwide ranked by ideXlab platform
Mingxing Jiang - One of the best experts on this subject based on the ideXlab platform.
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perforated patch recording of l type calcium current with beta escin in guinea pig ventricular myocytes
Acta Pharmacologica Sinica, 2003Co-Authors: Fang Wang, Hongyi Zhou, Xuesong Chen, Weixing Yao, Guojin Xia, Mingxing JiangAbstract:AIM: To establish a perforated patch recording (PPR) mode with beta-escin and compare L-type calcium current (I(Ca,L)) recorded under PPR and normal whole-cell recording (WCR) condition in isolated guinea-pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. beta-escin was added to the pipette solution to perforate the cell membrane and obtain PPR mode. I(Ca,L) was recorded using PPR and WCR techniques. RESULTS: beta-Escin 20, 25, and 30 micromol/L could permeabilize the cell membrane and obtain PPR mode. With beta-escin 25 micromol/L, the success rate was highest (16/17, 94 %) and the Time required for permibilization was 2-15 (8+/-4) min. Run-down of I(Ca,L) was considerably slower in PPR than in WCR condition. The amplitude of I(Ca,L) was decreased by 36 % at 20 min after the formation of WCR, while it was slowly decreased by 8 % at 30 min after the formation of PPR. The current-voltage relation (I-V) curves, activation and Inactivation curves of I(Ca,L) were not significantly different between WCR and PPR. The Inactivation rate of ICa,L was slower in PPR than in WCR, the faster Inactivation Time Constant (tau(f)) was longer in PPR than in WCR at membrane potentials of -20 mV -- +10 mV (n=6, P CONCLUSION: Using beta-escin 25 micromol/L can easily obtain stable PPR in isolated guinea-pig ventricular myocytes, and this method is useful in dealing with channels, which show run-down under normal WCR such as L-type Ca channel.
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effect of sea anemone toxin anthopleurin q on sodium current in guinea pig ventricular myocytes
Acta Pharmacologica Sinica, 2001Co-Authors: Liying Fu, Hongyi Zhou, Yang Li, Lan Cheng, Mingxing JiangAbstract:AIM: To investigate the effects of a sea anemone toxin anthopleurin-Q (AP-Q) isolated from Anthopleura xanthogrammica on sodium current (INa) in isolated guinea pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. INa was recorded using whole-cell patch-clamp technique. RESULTS: AP-Q (3 - 300 nmol/L) increased INa in a concentration-dependent manner. The EC50 value for increasing INa was 104 nmol/L (95 % confidence range: 78 - 130 nmol/L). AP-Q 300 nmol/L shifted the I-V curve to the leftward, changed the membrane potential of half maximal activation to more negative potential from (-36.3 +/- 2.3) mV to (-43 +/- 3) mV (n = 6, P < 0.01) and changed the membrane potential of half maximal Inactivation to more positive potential from (-75 +/- 6) mV to (-59 +/- 5) mV (n = 6, P < 0.01). AP-Q 300 nmol/L shortened the half-recovery Time of INa from (114 +/- 36) ms to (17 +/- 2) ms (n = 6, P < 0.01). The fast Inactivation Time Constant (tauf) of INa was markedly increased by AP-Q 300 nmol/L. CONCLUSION: AP-Q has a stimulating effect on I(Na) with slowing the Inactivation course of INa.
Andelain Erickson - One of the best experts on this subject based on the ideXlab platform.
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Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1
Scientific Reports, 2017Co-Authors: Marco C. Inserra, Mathilde R. Israel, Ashlee Caldwell, Joel Castro, Jennifer R. Deuis, Andrea M. Harrington, Angelo Keramidas, Sonia Garcia-caraballo, Jessica Maddern, Andelain EricksonAbstract:Human intoxication with the seafood poison ciguatoxin, a dinoflagellate polyether that activates voltage-gated sodium channels (Na_V), causes ciguatera, a disease characterised by gastrointestinal and neurological disturbances. We assessed the activity of the most potent congener, Pacific ciguatoxin-1 (P-CTX-1), on Na_V1.1–1.9 using imaging and electrophysiological approaches. Although P-CTX-1 is essentially a non-selective Na_V toxin and shifted the voltage-dependence of activation to more hyperpolarising potentials at all Na_V subtypes, an increase in the Inactivation Time Constant was observed only at Na_V1.8, while the slope factor of the conductance-voltage curves was significantly increased for Na_V1.7 and peak current was significantly increased for Na_V1.6. Accordingly, P-CTX-1-induced visceral and cutaneous pain behaviours were significantly decreased after pharmacological inhibition of Na_V1.8 and the tetrodotoxin-sensitive isoforms Na_V1.7 and Na_V1.6, respectively. The contribution of these isoforms to excitability of peripheral C- and A-fibre sensory neurons, confirmed using murine skin and visceral single-fibre recordings, reflects the expression pattern of Na_V isoforms in peripheral sensory neurons and their contribution to membrane depolarisation, action potential initiation and propagation.
Marco C. Inserra - One of the best experts on this subject based on the ideXlab platform.
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Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1
Scientific Reports, 2017Co-Authors: Marco C. Inserra, Mathilde R. Israel, Ashlee Caldwell, Joel Castro, Jennifer R. Deuis, Andrea M. Harrington, Angelo Keramidas, Sonia Garcia-caraballo, Jessica Maddern, Andelain EricksonAbstract:Human intoxication with the seafood poison ciguatoxin, a dinoflagellate polyether that activates voltage-gated sodium channels (Na_V), causes ciguatera, a disease characterised by gastrointestinal and neurological disturbances. We assessed the activity of the most potent congener, Pacific ciguatoxin-1 (P-CTX-1), on Na_V1.1–1.9 using imaging and electrophysiological approaches. Although P-CTX-1 is essentially a non-selective Na_V toxin and shifted the voltage-dependence of activation to more hyperpolarising potentials at all Na_V subtypes, an increase in the Inactivation Time Constant was observed only at Na_V1.8, while the slope factor of the conductance-voltage curves was significantly increased for Na_V1.7 and peak current was significantly increased for Na_V1.6. Accordingly, P-CTX-1-induced visceral and cutaneous pain behaviours were significantly decreased after pharmacological inhibition of Na_V1.8 and the tetrodotoxin-sensitive isoforms Na_V1.7 and Na_V1.6, respectively. The contribution of these isoforms to excitability of peripheral C- and A-fibre sensory neurons, confirmed using murine skin and visceral single-fibre recordings, reflects the expression pattern of Na_V isoforms in peripheral sensory neurons and their contribution to membrane depolarisation, action potential initiation and propagation.
Hongyi Zhou - One of the best experts on this subject based on the ideXlab platform.
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perforated patch recording of l type calcium current with beta escin in guinea pig ventricular myocytes
Acta Pharmacologica Sinica, 2003Co-Authors: Fang Wang, Hongyi Zhou, Xuesong Chen, Weixing Yao, Guojin Xia, Mingxing JiangAbstract:AIM: To establish a perforated patch recording (PPR) mode with beta-escin and compare L-type calcium current (I(Ca,L)) recorded under PPR and normal whole-cell recording (WCR) condition in isolated guinea-pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. beta-escin was added to the pipette solution to perforate the cell membrane and obtain PPR mode. I(Ca,L) was recorded using PPR and WCR techniques. RESULTS: beta-Escin 20, 25, and 30 micromol/L could permeabilize the cell membrane and obtain PPR mode. With beta-escin 25 micromol/L, the success rate was highest (16/17, 94 %) and the Time required for permibilization was 2-15 (8+/-4) min. Run-down of I(Ca,L) was considerably slower in PPR than in WCR condition. The amplitude of I(Ca,L) was decreased by 36 % at 20 min after the formation of WCR, while it was slowly decreased by 8 % at 30 min after the formation of PPR. The current-voltage relation (I-V) curves, activation and Inactivation curves of I(Ca,L) were not significantly different between WCR and PPR. The Inactivation rate of ICa,L was slower in PPR than in WCR, the faster Inactivation Time Constant (tau(f)) was longer in PPR than in WCR at membrane potentials of -20 mV -- +10 mV (n=6, P CONCLUSION: Using beta-escin 25 micromol/L can easily obtain stable PPR in isolated guinea-pig ventricular myocytes, and this method is useful in dealing with channels, which show run-down under normal WCR such as L-type Ca channel.
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effect of sea anemone toxin anthopleurin q on sodium current in guinea pig ventricular myocytes
Acta Pharmacologica Sinica, 2001Co-Authors: Liying Fu, Hongyi Zhou, Yang Li, Lan Cheng, Mingxing JiangAbstract:AIM: To investigate the effects of a sea anemone toxin anthopleurin-Q (AP-Q) isolated from Anthopleura xanthogrammica on sodium current (INa) in isolated guinea pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. INa was recorded using whole-cell patch-clamp technique. RESULTS: AP-Q (3 - 300 nmol/L) increased INa in a concentration-dependent manner. The EC50 value for increasing INa was 104 nmol/L (95 % confidence range: 78 - 130 nmol/L). AP-Q 300 nmol/L shifted the I-V curve to the leftward, changed the membrane potential of half maximal activation to more negative potential from (-36.3 +/- 2.3) mV to (-43 +/- 3) mV (n = 6, P < 0.01) and changed the membrane potential of half maximal Inactivation to more positive potential from (-75 +/- 6) mV to (-59 +/- 5) mV (n = 6, P < 0.01). AP-Q 300 nmol/L shortened the half-recovery Time of INa from (114 +/- 36) ms to (17 +/- 2) ms (n = 6, P < 0.01). The fast Inactivation Time Constant (tauf) of INa was markedly increased by AP-Q 300 nmol/L. CONCLUSION: AP-Q has a stimulating effect on I(Na) with slowing the Inactivation course of INa.
Charles N Allen - One of the best experts on this subject based on the ideXlab platform.
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tetraethylammonium tea increases the Inactivation Time Constant of the transient k current in suprachiasmatic nucleus neurons
Brain Research, 2008Co-Authors: Ludovic Alvado, Charles N AllenAbstract:Abstract Identifying the mechanisms that drive suprachiasmatic nucleus (SCN) neurons to fire action potentials with a higher frequency during the day than during the night is an important goal of circadian neurobiology. Selective chemical tools with defined mechanisms of action on specific ion channels are required for successful completion of these studies. The transient K + current ( I A ) plays an active role in neuronal action potential firing and may contribute to modulating the circadian firing frequency. Tetraethylammonium (TEA) is frequently used to inhibit delayed rectifier K + currents ( I DR ) during electrophysiological recordings of I A . Depolarizing voltage-clamped hamster SCN neurons from a hyperpolarized holding potential activated both I A and I DR . Holding the membrane potential at depolarized values inactivated I A and only the I DR was activated during a voltage step. The identity of I A was confirmed by applying 4-aminopyridine (5 mM), which significantly inhibited I A . Reducing the TEA concentration from 40 mM to 1 mM significantly decreased the I A Inactivation Time Constant ( τ inact ) from 9.8 ± 3.0 ms to 4.9 ± 1.2 ms. The changes in I A τ inact were unlikely to be due to a surface charge effect. The I A amplitude was not affected by TEA at any concentration or membrane potential. The isosmotic replacement of NaCl with choline chloride had no effect in I A kinetics demonstrating that the TEA effects were not due to a reduction of extracellular NaCl. We conclude that TEA modulates, in a concentration dependent manner, τ inact but not I A amplitude in hamster SCN neurons.
